The mechanism of oxidation-assisted initiation of surface cracks of a fourth-generation Ni-based single crystal superalloy was systematically investigated during low cycle fatigue at 900 °C and 980 °C. The results show that cracks initiate near the surface defects at 900 °C, while they initiate in the surface oxide layer at 980 °C. At 900 °C, the oxidation microcrack initiation in the thicker inner oxidation layer is difficult to connect with the surface oxidation crack, which is an essential reason for the crack growth rate being slower and not becoming the main crack. At 980 °C, microcracks form in the outer oxide layer and quickly connect with microcracks at the surface and inner/outer oxide layer interface, growing into long cracks that become channels for rapid oxygen transport. This accelerates the crack growth rate, and eventually the oxide crack becomes the main crack.

Total strain-control, low-cycle fatigue experiments of a fourth-generation Ni-based single-crystal superalloy were performed at 980 °C. Scanning electron microscopy and transmission electron microscopy are employed to determine fracture morphologies and dislocation characteristics of the samples. As the strain amplitude increased from 0.6 to 1.0%, the cyclic stress and plastic strain per cycle increased, the cyclic lifetime decreased, more interfacial dislocation networks were formed, and the formation rate accelerated. Cyclic hardening is associated with the reaction of accumulated dislocations and dislocation networks, which hinder the movement of dislocations. The presence of interfacial dislocations reduces the lattice mismatch between the γ and γ′ phases, and the presence of dislocation networks that absorb mobile dislocations results in cyclic softening. At a strain amplitude of 1.0%, the reaction of a high density of dislocations results in initial cyclic hardening, and the dislocation cutting into the γ′ phase is one of the reasons for cyclic softening. The crack initiation site changed from a near-surface defect to a surface defect when the strain amplitude increased from 0.6 to 0.8 to 1.0%. The number of secondary cracks initiated from the micropores decreased during the growth stage as the strain amplitude increased.